Case presentation on Pulmonary Edema Complicating Severe

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Case presentation on Pulmonary Edema Complicating
Severe Preeclampsia
Presented by Dr. Nicole Hodge Faculty
Advisor Dr. Norman Bolden
6 June 06
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Overview

• Severe preeclampsia pathophysiology, Dx,
  maternal/fetal issues, Treatment
• Standards of care and goals of anesthetic
  management
• Case - Ante partum flash Pulmonary edema
• Discussion

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PREECLAMPSIA

• A syndrome characterized by the new onset of
  hypertension and
• proteinuria after 20 weeks gestation. Additional
  signs and
• symptoms that can occur include edema, visual
  disturbances,
• headache, epigastric pain, thrombocytopenia, and
  abnormal liver
• function. These clinical manifestations are the
  results of
• mild to severe microangiopathy of target organs
  such as brain,
• liver, kidney, and placenta.

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PATHOPHYSIOLOGY OF PREECLAMPSIA

• A state of endothelial dysfunction secondary to
  excessive amounts of circulating factors released
  from the diseased placenta. These factors
  effect the establishment of a suitable vascular
  network of the placenta needed to supply oxygen
  and nutrients to the fetus.
• Molecular/Cellular level
• Abnormal expression of VEGF and sFlt-1 (Vascular
  endothelial growth factor proangiogenic and
  soluble fms-like tyrosine kinase 1-
  anti-angiogenic factors respectively) appear to
  play a central role.
• Increased expression of cytokines, angiotensin,
  catecholamines, and pro-coagulant factors.
• Anatomic level
• Increased vascular tone
• Increased vascular permeability
• Coagulopathy
• Ischemia of target organs (brain, liver, kidney,
  placenta)

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Multisystemic Disease

• CNS Cortical blindness, cerebral edema,
  cerebral hemorrhage, and seizures
• Cardiovascular Hypovolemia, increased SVR,
  LVH, increase sensitivity to catecholamines,
  sympathomimetics, and oxytocin
• Respiratory pulmonary edema, V/Q mistmatch,
  airway edema
• Renal Decreased renal blood flow, increased
  GFR, proteinuria, increased BUN and creatinine
• Hepatic subscabular hemorrhage, abnormal
  LFTs, decreased plasma cholinesterase levels
• Hematologic Prolonged bleeding time, platelet
  dysfunction, thrombocytopenia, DIC
• Placenta Uteroplacental insufficiency,
  placental abruption, chronic fetal hypoxia, IUGR,
  premature labor, premature birth.

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Diagnosis of Severe Preeclampsia

• If one or more of the following criteria are
  present
• Systolic blood pressure gt 160 mmHg
• Diastolic blood pressure greater than 110 mmHg
• Proteinuria greater than 5 g/24 hrs
• Evidence of end organ damage
• Oliguria (lt500ml/24hr)
• Cerebral or visual disturbances
• Pulmonary edema or cyanosis
• Epigastric pain or right upper-quadrant pain
• Impaired liver function
• Fetal growth restriction
• Thrombocytopenia

ACOG Compendium of Selected Publications
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Goals

• The goal of the anesthesiologist
• Control CNS irritability
• Magnesium sulfate anti-convulsant reduces
  irritability of the neuromuscular jxn.
• Restore intravasuclar fluid volume
• Strictly monitor urine output
• CVP monitor with goal 4-6 cm H20
• Normalize blood pressure
• Magnesium sulfate direct vasodilating action on
  smooth muscles of arterioles and uterus.
• Labetolol, Hydralazine, nifedipine, SNP (in
  extreme circumstances due to fetus susceptability
  to cyanide toxicity)
• Correct coagulation abnormalities
• Platelets, FFP, Cryoprecipitate

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Effects of Increasing Plasma Magnesium Levels

• MgSO4 in excess of therapeutic range
• Skeletal muscle weakness
• Respiratory depression
• Cardiac arrest (Ca can counter-act this)
• MgSO4 potentiates NMB and sedative effects of
  opiods
• Observed Condition mEq/L
• Normal Plasma level 1.5-2.0
• Therapeutic Range 4.0-8.0
• ECG Changes (Prolonged P-Q, widened QRS) 5.0-10
• Loss of deep tendon reflexes 10
• SA and AV node block 15
• Respiratory Paralysis 15
• Cardiac Arrest 25

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Anatomical Effects
Functional Effects
Functional effects
Increased respiratory drive
Airway edema friability
Minimal change in TLC Increased Minute
ventilation Reduced FRC
Widened AP and Transverse diameter
Increased cardiac output
Elevated Diaphragm
Normal diaphramatic Fxn
Widened Subcostal angle
Enlarging uterus
Increased O2 consumption and CO2 production
www.medtau.org
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Management

• Definitive treatment for Preeclampsia is delivery
  of the fetus and placenta.
• Vaginal Delivery Lumbar epidural
• No fetal distress
• Before catheter placement, r/o coagulopathy and
  insure adequate volume replacement.
• Cesarean Delivery Regional or GA
• Maternal/and or fetal status dictates the urgency
  for delivery
• Use epidural if in place. Maintain volume
  status. Typically, drops in BP improve placental
  blood flow.
• Spinal anesthesia, in the past, has been
  controversial due to possibility of severe
  hypotension. However, it has been shown to be a
  safe technique for cesarean delivery in severe
  preeclampsia.
• General anesthesia is an acceptable way to manage
  preeclamptic pts, however, there are associated
  risks.
• Apiration
• Airway compromise
• Cerebral hemmorrhage
• Pulmnary Edema

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Case Report

• 38 yo G1P0, 25 wks gestation, was transferred to
  MHMC/High Risk Pregnancy (from OSH) for
  management of acute on chronic hypertension
  (systolic gt200 mm Hg). Her pressures were
  stabilized with magnesium sulfate and
  hydralazine. No fetal distress. After approx.
  48 hrs., pt started to c/o of chest pressure and
  shortness of breath. Also intermittent episodes
  of variable decelerations/severe fetal
  bradycardia occurred. Cardiology consult with
  echocardiogram was obtained. Pt BP required prn
  labetolol. High risk team plan was to continue
  BP control and requested for anesthesia to place
  an arterial line.

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Case ReportAnesthesia Preoperative Assessment

• PMH/SH Chronic HTN, Anxiety, Depression/Breast
  biopsy
• MEDS Methyldopa 500mg po bid
• ALLERGIES Sulfa, erythromycin
• SH/FH quit smoking prior to conception/HTN
• ROS intermittent HA, occasional blurry vision,
  RUQ/epigastric, ankle swelling

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Case ReportAnesthesia Preoperative Assessment

• Exam
• VS BP-184/93, HR-94, R-22, T-37.0, SpO2 97,
  AOx3,No acute distress
• Airway exam - MPII, TMDgt4FW, FROM
• Cardiac RRR, no murmur appreciated, no JVD,
• Pulmonary CTA B
• Extremeties - 3 pedal edema
• Neuro grossly intact. No clonus
• Labs
• CMP 136/3.6/107/24/3/161 Mg 3.0
• CBC 9.62/10.7/32.8/289
• PT/PTT/INR 12.5/26.8/1.05
• TnI 0.38/0.37/0.39
• AST/ALT -16/16

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Case ReportAnesthesia Preoperative Assessment

• CXR (on admission)
• Heart is borderline in size. No focal infiltrate
  or pleural effusion is seen.
• The pulmonary vasculature is normal in
  appearance.
• Trans-thoracic Echocardiogram
• Dilated left atrium. Concentric left ventricular
  hypertrophy, significant mitral valve
  regurgitation, mild pulmonary hypertension (40-50
  mm Hg),
• LVEF -60
• ECG
• On admission (1/9/06) sinus tachycardia
• Day of consult (1/11/06) NSR, LAE

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Pre-operative Events

• The patient became extremely anxious and
  tachypneic after failed initial attempts at
  A-line placement. Base line sats 96-98. (recall
  h/o anxiety attacks)
• Put on 100 mask non-rebreather. Good color and
  breath sounds were clear bilaterally. Pulse
  oximetry was 91-97, but unreliable because she
  was moving around. Further attempts for A-line
  placement aborted until anxiety diminished.
• After approx 3-5 min, pt started complaining that
  her lungs were filling up. Auscultation
  revealed crackles to mid lung fields bilaterally.
  Sats decreased to 80. Airway supported with
  ambu bag.
• .

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CRISIS!!!

• A-line placed immediately, ABGs drawn.. Continued
  O2 support, PCXR ordered.
• BP 269/125 mmHg MAP 182 mmHg, HR-111
• ABG 7.28/48.8/70.4/90.2/22.2/-4.2
• CXR Opacities in mid and lower lung fields.
  Pulmonary edema.
• Increased distress/respiratory function worsened
  in supine position

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Anesthesia High Risk/OB Conference

• Assessment
• Severe Preeclampsia complicated by flash
  pulmonary edema
• Recent echo showed LVEF 60
• Pulmonary edema likely secondary to malignant
  hypertension
• Pts inability to lie supine lends immediate c/s
  technically difficult
• Fetal status reassuring
• Plan
• Continue
• Oxygen support
• BP control
• Monitor UOP
• Monitor ABGs
• Monitor Fetus
• When oxygenation is acceptable and patient can
  lie supine, proceed with c/s under regional,
  proceed with GA if BP intractable or fetal
  distress.

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Crisis Management

• Based on this information, O2 continued with
  100 NRB, BP was aggressively treated with
  Labetolol ( 120 mg). Lasix administered to
  resolve pulmonary edema.
• Continued monitoring of O2 sats
• Monitor UOP
• BPs under better control. NTG gtt started.
• ABG after 3 hours 7.411/37.5/174/99.0/23.4/-0.5
• Plan for c-section

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Intraoperative Events

• Pt in sitting position for prep/placement of
  epidural. Pt noted to have 3 pitting edema in
  lumbar area.
• 1 local and Touhy needle placed at L3-4. LOR,
  -heme/CSF. Catheter advanced easily. Negative
  aspiration. Test dose negative.
• Catheter was secured. Patient placed in supine
  w/left uterine displacement.
• Lidocaine 2 w/1200K epi and HCO3, total of 22
  ccs was given over 20 minutes. No sensory level
  was achieved.
• Anesthetic plan was converted to GA/RS
  Thiopental 250 mg, Sux 120 mg and Isoflurane.
• Surgeons proceeded with CS.

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Intraoperative Events

• MAC line was placed in the right internal jugular
  vein. CVP 20-30 mmHg.
• Swan-Ganz catheter placed. PAP avg 35/25 mmHg.
  Cardiac output not assessed due to equipment
  unavailability.
• Prior to delivery Sys gt170 / gt 100mmHg
• After delivery, Sys 110-170 /70-100 mmHg.
• Surgery completed w/o complication. Fluids LR
  500 ml, EBL 700, UOP 250.
• Pt remained intubated. Transferred to the CICU
  for cardiac care/post-op mgmt.

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Delivery of fetus
Delivery of Fetus
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Post-operative Events

• Pt was extubated POD1.
• Remained in ICU for several days for mgmt of BP
  and continued diuresis.

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Role of Invasive Hemodynamic Monitoring with
Severe Preeclampsia

• Most women with severe preeclampsia or eclampsia
  can be managed without invasive hemodynamic
  monitoring.
• A review of 17 women with eclampsia reported that
  use of a pulmonary artery catheter aided in
  clinical management decisions. (ACOG Compendium
  of Selected Publicatins J Clin Invest
  199391950-960)
• No randomized trials support their use in severe
  preeclamptic patients.
• Invasive hemodynamic monitoring may prove
  beneficial in preeclamptics with severe cardiac
  disease, renal disease, refractory hypertension,
  oliguria, or pulmonary edema. (ACOG Compendium of
  Selected Publications Am J Ostet Gyn 2000
  1821397-1403)
• Level III Research Opinions based on
  respected authorities, clinical experience,
  descriptive studies, or expert committees.

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Acute Pulmonary Edema in Pregnancy

• Cohort study 62,917 consecutive pregnancies
  from 1989-1999, to describe the incidence,
  predisposing factors contributing to pulmonary
  edema in the pregnant patient.
• Fifty-one women (0.08) were diagnosed with acute
  pulmonary edema during ante partum - post partum
  period.
• 24 patients (47) antepartum
• 7 patients (14) intrapartum
• 20 patients (39) post partum
• Most common causes
• Tocolytics (25.5) most commonly MgSO4 and SC
  terbutaline
• Cardiac disease (25.5)
• Fluid overload (21.5)
• Preeclampsia (18)

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Risk Factors

• Preeclampsia/eclampsia
• Tocolytic therapy
• Sever infection
• Cardiac disease
• Iatrogenic fluid overload
• Multiple gestation

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EBM Discussion on Anesthetic Technique for
Cesarean Section for Severe Preeclampsia

• Randomized comparison of general and regional
  anesthesia for cesarean delivery in pregnancies
  complicated by severe preeclampsia (1995)
• Eighty women who required C/S
• Randomized - epidural/CSE/General
• Intra-operative BP compared in all groups
• No statistical or clinical difference in maternal
  or fetal outcome
• Aside from logistical implications, general as
  well as regional were shown to be equally
  acceptable if steps are taken to ensure careful
  approach to either method.

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EBM Discussion on Anesthetic Technique for
Cesarean Section for Severe Preeclampsia

• Prospective cohort study Patients with severe
  preeclampsia experience less hypotension during
  spinal anesthesia for elective cesarean delivery
  than healthy parturients (2003).
• Compared incidence and severity of spinal
  anesthesia assoaicated hypotension in severe
  preeclamptic (n30) vs. healthy parturients
  (n30).
• Under spinal, mean BP decreased by 32-39 in
  severe preeclamptics and 33-60 in the healthy
  parturient.
• Healthy patients were given more ephedrine than
  the preeclamptics for hypotension. Possible
  explained by increased sensitivity of pressor
  drugs in the preeclamptic.
• Findings suggest that the incidenc of severity of
  spinal hypotension in preeclamptic patients with
  severe hypertension may be less than previously
  believed.

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Discussion

• Most likely cause of pulmonary edema is
  multifactorial. No specific etiology was
  assigned.
• Unsuspected cardiac findings were common, and
  there was a high incidence of valvular disease.
• Most pts had severe systolic dysfunction and LVH
  and not cardiac disease.
• Underlying cardiac disease is most likely
  under-diagnosed and under-reported due to
  under-use of echocardiography.

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References

• Journals
• A. Sciscione et al. Acute Pulmonary Edema in
  Pregnancy. Obstetrics Gynecology
  2003103511-14.
• D. Wallace et. al. Randomized Comparison of
  General and Regional Anesthesia for Cesarean
  Delivery in Pregnancies Complicated by Severe
  Preeclampsia. Obstetrics Gynecology
  199586198-98.
• A. Aya et al. Patients with Severe Preeclampsia
  Experience Less Hypotension During Spinal
  Anesthesia for Elective Cesarean Delivery than
  Healthy Parturients A Prospective Cohort
  Comparison. Anesthesia Analgesia
  200397867-72
• Texts/Other
• Baresh, Paul G. Clinical Anesthesia.
• Stoelting, R. Anesthesia and Coexisting Disease
• Up to Date www.uptodate.com keyword severe
  preeclampsia

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Questions????